Rapid sequence induction (RSI) for intubation is an effective method for securing the airway in combative or agitated patients.
If hypotension is detected at any time in the course of the emergent management of a head-injured patient, a cause should be sought other than the head injury. Hypotension is rarely caused by head injury except as a terminal event, but important exceptions include profound blood loss from scalp lacerations and pediatric patients with relatively small circulating blood volumes. In small children, hemorrhage into an epidural or subgaleal hematoma can produce profound hypovolemic shock. In the presence of concomitant spinal cord injury, spinal cord hypotension may occur. This is rare and can be differentiated from hypovolemic hypotension by its nonresponsiveness to fluid administration.
Recently, it has been suggested that hypotensive patients with penetrating abdominal trauma may have better outcomes if fluids are restricted before operation. These studies did not include head-injured patients. In the case of the head-injured patient, systematic hypotension cannot be tolerated without profound worsening of neurologic outcome; fluids should therefore be delivered to maintain a systolic blood pressure of at least 90 mm Hg. Several laboratory and clinical studies have investigated the effects of the delivery of large amounts of fluid to severely head-injured patients who are hypotensive from other injuries and have not demonstrated clinically significant increases in ICP. Fluids should not be withheld in the hypovolemic hypotensive head trauma patient for fear of increasing cerebral edema and ICP. Hypotension from any cause increases mortality from the head injury by 30%. Hypotension may interfere with the accurate neurologic assessment of the brain-injured patient. Often, when blood pressure is restored, an improved neurologic status is observed.
As many as 60% of patients with severe head injury are victims of multiple trauma. The dramatic presentation of the head injury should not distract the clinician from a thorough search for other life threats.
The ED neurologic assessment should be compared with the initial prehospital examination, focusing on evidence of neurologic deterioration or signs of increasing ICP. If the patient is deteriorating or has signs of increased ICP, active intervention must be initiated in the ED.
Hyperventilation to produce an arterial P CO2 of 25 to 30 mm Hg will temporarily reduce ICP by promoting cerebral vasoconstriction and subsequent reduction of CBF. The onset of action is within 30 seconds and probably peaks within 8 minutes after the P CO2 drops to the desired range. In most patients hyperventilation lowers the ICP by 25%; if the patient does not rapidly respond, the prognosis for survival is generally poor. Prolonged hyperventilation probably loses its effectiveness and therefore is of limited value beyond the acute phase. The partial pressure of carbon dioxide should not fall below 25 mm Hg because this may cause profound vasoconstriction and ischemia in normal and injured areas of the brain. Prophylactic hyperventilation has been associated with worsened neurologic outcome when measured at 3 and 6 months after severe trauma and is therefore not recommended in head-injured patients who are not exhibiting signs of increased ICP.